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RESEARCH HIGHLIGHTS
Nature Reviews Gastroenterology & Hepatology 10, 260 (2013); published online 2 April 2013; doi:10.1038/nrgastro.2013.58

HEPATOCELLULAR CARCINOMA

Actopaxin has a role in HCC metastasis
Previous studies have shown that
actopaxin, a focal adhesion protein, is
involved in cell migration, invasion and
matrix degradation, which are important
steps in cancer metastasis. Owing
to these findings, Roberta Pang and
co-workers from the University of Hong
Kong felt confident that this protein
might have a role in hepatocellular
carcinoma (HCC) metastasis and
decided to investigate their theory.
The researchers used three lines
of investigation in their study: first,
they examined actopaxin expression
in samples from patients with HCC;
second, they investigated whether
actopaxin regulates cellular processes
that lead to metastasis (such as cell
migration and invasion) in an HCC cell
line; and third, the researchers studied
the effects of actopaxin repression on
HCC metastasis in vivo.
Actopaxin was found to be frequently
overexpressed in patients with HCC,

and overexpression correlated with the
development of metastases. Suppression
of actopaxin was found to impair HCC
metastasis in the cell line and the mouse
models. Moreover, downregulation of
actopaxin in the HCC cell line enhanced
the chemosensitivity of these cells.
The authors are hopeful that actopaxin
might be a potential therapeutic target
in HCC. “Data from this study provide
concrete evidence of an important role
of actopaxin in HCC progression and
metastasis,” says Pang. “We believe that
further work on actopaxin suppression
will be beneficial for combating metastasis
and chemoresistance in HCC, and
hopefully in other types of cancer.”
Isobel Leake
Original article Ng, L. et al. Suppression of actopaxin
impairs hepatocellular carcinoma metastasis through
modulation of cell migration and invasion. Hepatology
doi:10.1002/hep.26396

NATURE REVIEWS | GASTROENTEROLOGY & HEPATOLOGY 	
© 2013 Macmillan Publishers Limited. All rights reserved

VOLUME 10  |  MAY 2013

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Nrgastro.2013.58

  • 1. RESEARCH HIGHLIGHTS Nature Reviews Gastroenterology & Hepatology 10, 260 (2013); published online 2 April 2013; doi:10.1038/nrgastro.2013.58 HEPATOCELLULAR CARCINOMA Actopaxin has a role in HCC metastasis Previous studies have shown that actopaxin, a focal adhesion protein, is involved in cell migration, invasion and matrix degradation, which are important steps in cancer metastasis. Owing to these findings, Roberta Pang and co-workers from the University of Hong Kong felt confident that this protein might have a role in hepatocellular carcinoma (HCC) metastasis and decided to investigate their theory. The researchers used three lines of investigation in their study: first, they examined actopaxin expression in samples from patients with HCC; second, they investigated whether actopaxin regulates cellular processes that lead to metastasis (such as cell migration and invasion) in an HCC cell line; and third, the researchers studied the effects of actopaxin repression on HCC metastasis in vivo. Actopaxin was found to be frequently overexpressed in patients with HCC, and overexpression correlated with the development of metastases. Suppression of actopaxin was found to impair HCC metastasis in the cell line and the mouse models. Moreover, downregulation of actopaxin in the HCC cell line enhanced the chemosensitivity of these cells. The authors are hopeful that actopaxin might be a potential therapeutic target in HCC. “Data from this study provide concrete evidence of an important role of actopaxin in HCC progression and metastasis,” says Pang. “We believe that further work on actopaxin suppression will be beneficial for combating metastasis and chemoresistance in HCC, and hopefully in other types of cancer.” Isobel Leake Original article Ng, L. et al. Suppression of actopaxin impairs hepatocellular carcinoma metastasis through modulation of cell migration and invasion. Hepatology doi:10.1002/hep.26396 NATURE REVIEWS | GASTROENTEROLOGY & HEPATOLOGY © 2013 Macmillan Publishers Limited. All rights reserved VOLUME 10  |  MAY 2013